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imed3004 > Endocrine Pathology: Thyroid Gland > Flashcards

Endocrine Pathology: Thyroid Gland Flashcards

1
Q

What is iodine used for in thyroid gland function?

A

2 active thyroid hormones, require iodine for formation: Thyroxine (T4) and 3,5,3’-triiodothyronine (T3)

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2
Q

How are thyroid hormones carried in the blood?

A

Via carrier proteins in the serum. (Thyroxin-binding globulin, transthyretin, albumin, and lipoproteins)

The bound hormone represents a circulating storage pool and unbound hormone is active.

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3
Q

Which hormones act on tissues and how?

A

T3 is more active than T4 and there is variability in tissue action based on tissue distribution of receptors (2 main receptors, alpha and beta)

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4
Q

Is thyroid disease always symptomatic?

A

No, a wide range of processes lead to the same symptomatology. Diagnosis needs to consider anatomical and biochemical factors as well as time course and pathological processes.

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5
Q

What is the possible disease aetiologies for thyroid pathology?

A

VITAMIN C

Vascular

Inflammatory / Infective

Trauma

Autoimmune

Metabolic

Iatrogenic / Idiopathic

Neoplastic

Congenital / Genetic

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6
Q

What are the clinical consequences of thyroid disease?

A

Mechanical / Anatomical: Thyroid enlargement (goitre), compression effects, thyroid enlargement is not usually painful.

Functional / Hormonal: Euthyroid, hyperthyroidism, hypothyroidism

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7
Q

What causes hyperplasia of thyroid gland?

A

Diffuse / Grave’s disease (Autoimmune)

Multinodular goitre / Nodular colloid goitre

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8
Q

What conditions are neoplastic in the thyroid gland?

A

Adenomas (Benign): Follicular

Carcinomas (Malignant): Papillary, follicular, anaplastic, medullary

Inflammatory: Hashimoto

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9
Q

What are the 4 types of malignant thyroid carcinomas?

A

FAMP

Follicular

Anaplastic

Medullary

Papillary

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10
Q

What results from hypothyroidism most commonly in infancy/childhood?

A

Cretinism (Usually endemic environmental or dietary iodine deficiency)

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11
Q

What causes cretinism in children?

A

Hypothyroidism caused by endemic environmental or dietary iodine deficiency.

Can be caused by rare inborn errors of metabolism

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12
Q

How does cretinism happen?

A

Impaired development of skeleton and CNS resulting in short stature, coarse facial features, protruding tongue, umbilical hernia, and severe mental impairment.

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13
Q

Does hypothyroidism in the mother affect the foetus?

A

Yes

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14
Q

How common is hypothyroidism in adults?

A

0.3% but subclinical estimated to be approx. 4%

10x more common in women than men

More common at ages >60

May result from defects anywhere in the HPT axis

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15
Q

What are the causes of primary hypothyroidism?

A

Genetic defects in thyroid development (PAX8, FOXE1, TSH receptor mutations)

Thyroid hormone resistance syndrome

Autoimmune hypothyroidism (hashimoto)

Iodine deficiency

Drugs

Congenital biosynthetic defect (dyshormonogenetic goiter)

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16
Q

What are the causes of secondary hypothyroidism?

A

Pituitary failure

Hypothalamic failure

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17
Q

What are the clinical signs and symptoms of hypothyroidism?

A

Chronic hypothyroidism leads to myxoedema

Slowing of physical and mental activity (fatigue, cold intolerance, overweight, low sympathetic activity and cardiac output)

Drop in T4 leads to increase in TSH (this differentiates primary hypothyroidism from secondary hypothyroidism)

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18
Q

What causes hashimoto’s thyroiditis?

A

Autoimmune disease - breakdown of self tolerance to thyroid antigens. (HLA-DR5 and HLA-DR3)

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19
Q

Who gets hashimoto’s thyroiditis most commonly?

A

Occurs at any age including children predominantly in females.

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20
Q

What causes hashimoto’s thyroiditis?

A

Inciting events are not clear but seem to involve abnormalities in T cells due to exposure of normally sequestered thyroid antigens.

This disease sometimes overlaps with other autoimmune thyroid diseases like Grave’s disease and other endocrine organs.

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21
Q

How are people treated with hashimoto’s thyroiditis?

A

No cure at the moment so treatment is hormone replacement

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22
Q

What are the histopathological features of hashimoto’s thyroiditis?

A

Diffuse lymphoid (and plasma cell) infiltrates with reactive lymphoid follicles.

Degeneration and apoptosis of epithelial cells with oncocytic changes (Hurthle cells)

Gland normal size or slightly small

Later atrophy, fibrosis

Slightly increased risk of lymphoma and slightly increased risk of carcinoma

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23
Q

What are the symptoms of hyperthyroidism?

A

Nervousness, anxiety

Heat intolerance

Palpitations

Tachycardia and atrial arrhyhtmia

Systolic hypertension with wide pulse pressure

Lid lag

Muscle weakness

Weight loss despite increased appetite

Menstrual issues

24
Q

What does hyperthyroidism lead to?

A

Thyrotoxicosis which is a hypermetabolic state due to excess T3/T4

25
Q

What are the most common causes of hyperthyroidism?

A

Diffuse hyperplasia (Graves disease)

Hyperfunctional MNG

Hyperfunctional thyroid adenoma (most carcinomas are non-functional)

26
Q

What are the less common causes of hyperthyroidism?

A

Hashitoxicosis (early hashimotos)

Iodine overload

Central (TSH mediated)

Paraneoplastic: Germ cell tumours and inappropriate TSH secretion.

Drugs

27
Q

How are symptoms often different between young people and older people with hyperthyroidism?

A

Younger people get the symptoms of overactive sympathetic nervous system (tremors, anxiety, etc)

Olderpatients tend to have more CVS symptoms and unexplained weight loss

28
Q

Who gets grave’s disease most often?

A

Women 20 - 40 years of age.

Common (1 - 2% of people)

Can be subclinical in many people.

Genetic factors so familial

29
Q

What happens in Grave’s disease?

A

It is autoimmune with autoantibodies being produced against the TSH receptor and other thyroid antibodies.

These antibodies activate the receptors and so leads to hyperthyroidism. (Antibodies are called Thyroid stimulating Imunoglobulins TSIs)

Minority get hypothyroidism due to TSH blocking antibodies.

Thyroid gets very large which leads to functional symptoms and mass effect.

Leads to bulging eyes. (Periorbital oedema, lid lag, lid retraction, diplopia, proptosis)

30
Q

What are the histopathological features of grave’s disease?

A

Epithelial hypertrophy and hyperplasia with papillary formations and “scalloped” colloid.

Gland usually 100 - 159g, but may be much larger.

Doesn’t have the features of a neoplasm.

31
Q

What is pretibial myxoedema?

A

It is the accumulation of myxoid mucopolysaccharides in subcutaneous tissue

32
Q

What are nodular colloid goitre?

A

Simple colloid goitre arises sporadically which occurs from iodine deficiency. Reduced iodine leads to reduced hormone production which leads to hyperplasia of thyroid follicles due to stimulation by TSH to work “harder”

This then transitions to late stage nodular colloid goitre. During this stage there are cycles of hyperplasia and involution which lead to nodule formation, with some areas demonstrating benign clonal proliferation then this goitre degenerates.

33
Q

What are goitrogens?

A

Foods that can contribute to goitre formation such as cabbage, cauliflower, broccoli, kale, etc

34
Q

What percentage of thyroid neoplasms are malignant?

A

Less than 1% of solitary thyroid nodules are malignant. Most thyroid cancers (90% live >20 years) are low stage and papillary.

35
Q

What kind of thyroid nodules are more likely to be neoplastic?

A

Solitary more likely than multiple

Younger patients more likely than older patients (better prognosis for young people if malignant)

Males more likely than females

Nodules that take up radioactive iodine in imaging studies are more likely to be benign than malignant

36
Q

What kind of thyroid nodules are associated with history of radiation exposure?

A

Malignant nodules.

37
Q

What are the types of thyroid neoplasms that affect the thyroid gland?

A

Adenomas (benign epithelial tumours): most are follicular

Carcinomas (Malignant epithelial tumour): Follicular, papillary (most common type), anaplastic, medullary carcinoma

38
Q

What are the histological features of adenomas?

A

Most are follicular, solitary, well circumscribed, encapsulated, with normal thyroid background.

Important: No capsular invasion, extrathyroidal extension or lymphovascular invasion

Majority are non functional

39
Q

How are thyroid adenomas treated?

A

Hemithyroidectomy

40
Q

What are the histological features of follicular carcinomas?

A

Similar radiological appearance and presentation to follicular adenoma (hurthle cell carcinoma is less common)

Solitary nodule

Well or poorly circumscribed

Thickly incapsulated

Capsular invasion, extrathyroidal extension or lymphovascular invasion (minimal = good widely = bad)

Majority are non-functional and may metastasize late

41
Q

What kind of spread do follicular carcinomas have?

A

Haematogenous spread: Bones, lungs, liver

42
Q

What kind of mutations result in follicular carcinoma?

A

PAX8 and RAS/PI-3K mutations

43
Q

What is the most common thyroid cancer?

A

Papillary carcinoma

44
Q

Who often presents with papillary carcinoma?

A

Often young women

45
Q

What is treatment for papillary carcinoma and why?

A

Total thyroidectomy due to it often being multifocal.

46
Q

What does a papillary carcinoma look like histologically?

A

Forms papillae with crowded cells demonstrating nuclear grooves and clear chromatin. often psammomatous calcification and fibrosis (not encapsulated)

47
Q

What kind of invasion is common for papillary carcinomas?

A

Lymphatic invasion (to central neck nodes)

48
Q

What kind of mutations are papillary carcinomas associated with?

A

RET/PTC or BRAF mutations (activate MAPK pathway)

49
Q

What is the prognosis like in papillary carcinomas?

A

Good prognosis (worse in older patients)

50
Q

What is an anaplastic carcinoma?

A

Rare carcinoma seen in older patients (65+) that is aggressive, rapidly enlarging and infiltrative neck mass with mass effect leading to hoarseness.

51
Q

What are the histological features of anaplastic carcinoma?

A

Often mets at time of presentation

Often multifocal

Anaplastic

Pleomorphic cells

Mix large and small cells, multinucleation

Spindled

Lose markers of thyroid differentiation by immunohistochemistry

Lymphatic invasion is common and lung metastases.

52
Q

What kind of invasion is anaplastic carcinoma associated with?

A

Lymphatic invasion

53
Q

What mutation are medullary carcinomas associated with?

A

MEN2. Nearly 100% risk in families with it.

Express neutoendocrine markers and calcitonin by immunohistochemistry.

54
Q

What is a medullary carcinoma?

A

Neuroendocrine carcinoma of thyroid gland.

Originates from C cells and may be preceded by C-cell hyperplasia.

55
Q

Does medullary carcinoma produce hormones?

A

Yes, most secrete calcitonin and have amyloid in stroma

56
Q

How do medullary carcinomas metastasize?

A

Behaviour is variable. They metastasize via lymphatics or blood vessels (65% 10 year survival rate much better if detected early)

57
Q

How is pathology testing done with thyroid neoplasia?

A

Hormonal assay (TSH, Free T3/T4)

Anti-thyroid antibodies (if autoimmune disease suspected)

Serum calcitonin

FNA cytology

Frozen section

Histopathology +/- immunohistochemistry

Genetic screening if MEN suspected

imed3004 (50 decks)

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